Psychotropic drugs
chemical substances that change brain function and result in alterations in perception, mood, consciousness or behavior
Psychotherapeutic agents
licensed psychotropic drugs exerting therapeutic benefit
Psychomimetics
affects psyche without therapeutic value (MDMA)
What are psychotherapeutic agents for
mania
anxiety disorder
unipolar depression
lithium
benzodiazepines
antidepressants
what are the key symptoms for depression?
depressed mood
apathy
How does Reserpine affect monoamines in the brain?
Reserpine blocks VMAT, preventing monoamines from entering vesicles.→ They remain in the cytoplasm and are broken down by MAO, leading to decreased neurotransmitter levels and potential depressive symptoms.
How does Iproniazid act as an antidepressant?
It’s a monoamine oxidase inhibitor (MAOI) that blocks the breakdown of serotonin, dopamine, and norepinephrine,→ increasing their levels in the brain and improving mood.
What is the role of monoamine oxidase (MAO)?
MAO is an enzyme that breaks down monoamine neurotransmitters like serotonin, dopamine, and norepinephrine.There are two types: MAO-A (serotonin, NE) and MAO-B (mainly dopamine).
How do TCAs affect serotonin?
They inhibit the reuptake transporter, so more serotonin stays in the synaptic cleft, leading to stronger serotonergic signaling
What do tricyclic antidepressants (TCA) do?
They block the reuptake of serotonin(5-HT) and norepinephrine(NA), increasing their levels.→ Effective but have many side effects due to broad receptor binding.
How do SSRIs treat depression?
SSRIs selectively block serotonin reuptake, increasing serotonin levels with fewer side effects than older drugs like TCAs.
What does α-Methyltyrosine (AMPT) do?
It inhibits tyrosine hydroxylase, blocking the synthesis of dopamine, norepinephrine, and epinephrine, leading to worse mood
what is the contra of TCA?
mood elevation delayes
How does monoamine deficiency affect receptors in depression?
upregulation of postsynaptic monoamine neurotransmitter receptors
leads to increased sensitivity for NA, DA and 5-HT
Why do TCAs have many side effects?
Because they block M1 (ACh), H1 (Histamine), and α1 (NE) receptors —→ causing sedation, weight gain, dry mouth, and low blood pressure.
Nane four advantages of SSRI over TCA?
less sedation
less anticholinergic effects
less arrythmias
lower risk od intoxication
What does an α₂-antagonist do?
It blocks presynaptic α₂-receptors, lifting the brake on noradrenaline release —→ leading to increased NA levels and potential antidepressant or activating effects.
Another word for neuroleptics
antipsychotics
What is schizophrenia
disorders of thinking, perception and affect the reltionship to the environment
what was the first antipsychotics for schizophrenia
chlorpromazine
developed as anthistamine for surgery sedatioon
What are the reasons for schizophrenia
a mixture of:
genetic
dopamin-hypothese ( over and under activity)
development of brain
what are reasonable grounds for the dopamine hypthesis (schizophrenia is due to an enhancement of dopaminegic activity) of schizophrenia
effects of antipsychotics
post mortem examination of brain -> increased amount of dopamine receptors
amphetamine-induced psychosis
What role does the mesolimbic dopamine pathway play in schizophrenia and which brain areas does it affect?
It’s overactive in schizophrenia,→ leading to positive symptoms like hallucinations and delusions.
(VTA-> limbisches System)
Antipsychotics block D₂ receptors here to reduce these effects.
What is the mesocortical dopamine pathway associated with in schizophrenia and which brain areas does it affect?
It’s underactive,→ causing negative symptoms like flat affect, apathy, and poor concentration.
VTA → präfrontaler Kortex
D₂-blocking drugs may worsen these symptoms.
Which two dopamine pathways you know besides mesolimbic and mesocortical?
nigrostriatal (substantia nigra -> striatum)
involved in coordination of movement
tuberoinfundibular (hypothalamus -> hypophyse)
regulates secretion of prolactin
What three pieces of evidence support the dopamine hypothesis of schizophrenia?
Amphetamines cause psychotic symptoms in humans
Bromocriptine (D₂ agonist) alters behavior in animals
Antipsychotic potency correlates with D₂ receptor affinity
What two contras for the dopamine hypothesis of schizophrenia?
lack of evidence for elevated dopamine metabolites
lateny of antipsychotics-induced effects
How do serotonin receptors extend the dopamine hypothesis?
Overactive 5-HT₂A receptors may contribute to hallucinations and modulate dopamine.Atypical antipsychotics block both D₂ and 5-HT₂A for better effect.
How does glutamate extend the dopamine hypothesis?
NMDA receptor hypofunction may drive dopamine imbalance, causing positive and negative symptoms.Glutamate may act as an upstream regulator of dopamine.
What is an endocrine effect in psychopharmacology?
A hormonal change caused by a drug,e.g. elevated prolactin due to D₂-blockade by antipsychotics → causing amenorrhea, galactorrhea.
what makes an antipsychotic atypcial - pharmacologically?
d2 antagonist
5HT2A antagonist
binding affinity: D2 <5GT2A
d2/5H1A partial agonist
what makes an antipsychotic atypcial - clinically?
imporves effectivness against negativ symptoms
reduced occurence of dyskinesia
What are extrapyramidal symptoms (EPS)?
Drug-induced movement disorders caused by D₂ blockade in the nigrostriatal pathway,including Parkinsonism, akathisia, dystonia, and tardive dyskinesia.
conventional AP vs atypical?
conventional:
d2 antagonism
high efficacy against pos symptoms (lowe for neg symptoms)
inference(störung) with cog functions
atypical:
d2/5HT2A antagonism
efficient against pos and neg symptoms
pos influence on cognition
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